It is believed T wave alternans is a marker of impending ventricular fibrillation. Though it is not applicable in every clinical setting it is indeed true if we observe T wave alternans in an acute ischemic setting .Here is a patient with ACS and inferior MI who developed T wave alternans after temporary pacing.

went in for a chaotic T wave rhtythm and ended up in VF that required s shock.T wave alternans is other wise known as repolarisation alternans .

Twist dance of Heart

Torsedes is twist around it’s axis. Any ECG wave can twist in it’s axis .If T wave alternans becomes gross it will twist 180 degrees .Once this happens the heart can go for fibrillation any moment !

Final message

Extreme form of T wave alternans would result in complete twisting of repolarization vector which is a harbinger of ventricular fibrillation

I wish this can be referred to as Torsades “T” pointes instead of Torseades “de” pointes

Thrombus laden plaque is sine qua-non of UA/NSTEMI . That’s what we have been taught ! right ? It may be true in many situations , but please remember there is another concept called demand ischemia , where in there is no active thrombus , still resting angina may occur due to increasing heart rate etc.

I just wanted to test how far this concept is understood , by the fellows in our coronary care unit . Following is story of a patient who arrived at CCU with angina at rest . I showed this ECG asked them the management .

History was purposefully blinded . 5/6 cardiologists wanted to admit the patient either in CCU or rush to cath lab. Heparin/ Fondaparuinux was prescribed by all. Tirofiabn was suggested by few.It is a high risk UA with left main disease some one mumbled .

I silently listened to them and revealed the history . This patient has just finished the exercise stress test , it was terminated as he had angina at peak exercise. and was reported as positive . A date was fixed for elective coronary angiogram. 10 minutes later ECG totally normalised , and the patient went home (Boarding a crowded Chennai city bus )

The fellows realised the importance of history . In fact no body asked for it ? I felt bad as all my fellows failed in this test That reflects bad teaching on my part !

What is the mechanism of ST depression here ?

Fresh thrombus ?

Mechanical occlusion ?

High heart rate ?

Combination of high rate and probable flow limiting lesion .

(Severe forms of stable angina can occur at rest . So do not equate all rest angina as true unstable angina !)

Final message

Do not label an ECG straightaway as acute coronary syndrome when there is baseline tachycardia and ST depression . Spare few minutes and apply your mind !

If a combination of ST depression and angina can be taken synonyms with UA every EST positive fellow should be labeled as UA and admitted in CCU. Please remember any tachycardia with a fixed tight lesion will mimic UA . Further , since there is no thrombus here and there is absolutely no role for heparin.

ST segment elevation is the key parameter on which the fate of millions of infarct patients are recognised and managed. It is ironical we do not have standardised reference point for measuring the quantum of SR elevation .

This is especially difficult when ST segment blends with forward limb of T waves.

While we have reference point for measuring ST depression (Like during EST ). . . why we do not have one for ST elevation ?

Now we have adopted a rough criteria .Read below .

How to measure ?

Measure The ST segment 40 ms from J point.

I lost track the source of this Image .(STEMI hand book 2012 ?)

Final message

ST segment elevation is the key parameter in ACS. Quantifying it becomes important in assessing the efficacy of reperfusion strategies and risk stratification. Fresh ST elevation can represent pericarditis, reinfarction or an early dyskinetic segment . Unless we have proper reference point there is a room for error in this simple parameter.

95 % of hypertension is designated as primary HT .What does it mean ? It means 95 % of times we do not know what exactly is the cause for raised blood pressure . Simply stated . . . it reflects 95% ignorance .

So what is secondary hypertension ?

Secondary HT is the one, in which we have specific reason for the raised BP. The most important cause is Renal , endocrine etc.

Heart disease was once considered as rich man’s disease . . . It’s no longer true . We in India , are witnessing an epidemic of CAD . The reasons are varied . Apart from conventional factors , social factors like changing demographic pattern , life style , ethnic risk like south Asian metabolic profile are responsible .

While Rheumatic heart disease (RHD ) continues to be a huge burden , CAD is the number one cause for cardiovascular morbidity and mortality .

CAD affect the poor and rich with equal vengeance . The later is better equipped financially to tackle it . Of course , it has resulted in maximum inappropriate interventions. The poor (or borderline poor ) have no other option but to knock the doors of Government hospitals. It is heartening to note, various state Governments are gradually involving insurance schemes.

Still , many struggle to find the required finance for a major cardiac intervention. It roughly costs 100,000 rupees for PTCA .While PCI is required in all symptomatic , critical coronary occlusions , still . . . majority of the CAD in general population do not require it . There are 675 cath labs in India performing 180000 angioplasties every year on an average of 15000 PCI per month ( 500 /day ) This is grossly inadequate . We have huge potential

What is the hurdle ?

Expertise ?

Hard ware ?

Awareness ?

No . . . it is all about financial resources

Recently I stumbled upon an advertisement on Times of India

Disclaimer: This article does not in any way defame any hospital that offers the scheme.It just want to debate the concept.

Hospitals want to market the procedure . Convert angiograms to angioplasties . That’s corporate boardroom mantra . And one fine day , bankers and medical doctor sat together and brought a brilliant idea.

Why not do the procedure on credit and push the patient life long into a financial debt !

Financing a poor patient with good intention is welcome. But, there is big caveat .In a vast country with high illiteracy , inappropriate procedures may be thrusted upon on the poor souls.

After thought

Now , our patients have one more risk parameter to assess ” Number of remaining EMI( Equal monthly instalment ) and incidence of stent thrombosis” “Accumulated interest and angina” What a wonderful way to provide cardiac care !

I can recall a patient who sold his livestock (his sole income source ) for undergoing a open heart surgery and lost his life as well in the process leaving the family stranded !

Solution

The only solution is to provide a strictly regulated Govt sponsored insurance scheme. High tech procedures should be continuously and meticulously audited for cost effectiveness .